Abstract

Elucidation of the respective functional roles of the D1 and D2 subtypes of dopamine receptors in the basal ganglia has been the subject of intense study in recent years. According to the definitions proposed by Kebabian and Calne (1979), D1 receptors stimulate adenylate cyclase, and D2 receptors either inhibit or have no effect on this enzyme. Until the last few years, no function was ascribed to the D1 receptor. Neuroleptics, drugs used to treat psychosis, are all antagonists at D2 receptors, although some are also antagonists at D1 receptors. Supersensitivity of D2 receptors has been proposed as the basis for tardive dyskinesia, a hyperkinetic involuntary movement disorder that may develop after long-term administration of neuroleptics. Dopamine agonists exacerbate tardive dyskinesia (Tarsy & Baldessarini, 1977) and administration of neuroleptics to rats results in an increase in the density of striatal D2 receptors (e.g., Burt et al., 1977).